Information

Why don't all bacteria have F-plasmids by now?


Some bacteria can undergo gene transfer by conjugation. Conjugation is a form of horizontal gene transfer, meaning from one (unrelated) bacterium to another (in contrast to vertical gene transfer, which is from predecessor bacterial cell to successor (daughter) cells). Conjugation is initiated when one bacterium has an F-plasmid (Fertility plasmid) and forms an F-pilus, connecting the F+ bacterium with an F- bacterium, initiating transfer of the F-plasmid.

Why is it that during evolution not all bacteria have acquired this F-plasmid?


Conjugation occurs between cells of the same species too. For this to occur cell have to be close to each other. Now, if you have an isolated population of bacteria that never gets in contact with an F+ bacteria then this population would stay F-. Also not all conjugation events are successful, mechanical perturbations can disrupt the pilus through which genetic material is transferred. This old article can give you good details: THE ORIGIN OF BACTERIAL SPECIES - GENETIC RECOMBINATION AND FACTORS LIMITING IT BETWEEN BACTERIAL POPULATIONS ARNOLD by W.RAVIN

F+ shares, however, an important property of bacteriophage: after infection it behaves as though it were an addition to the bacterial genome. As an addition, it can furthermore exist in one of two forms: in one form, it is an unintegrated part of the bacterial genome, and may be replicated either more or less rapidly than the "chromosomal" or linked genes (being infectious or lost through dilution, respectively); in its other form, it is integrated in the sense that its replication is coordinated with the replication of the host's genes, as though attached to them. In this latter form, found in Hfr bacteria, the F+ factor is incapable of infecting other bacteria (while permitting conjugation with them) and also prevents superinfection of its host bacterium by a nonintegrated F+ factor.

Taken from the linked paper. So you can see that are situations where conjugation occurs yet the F- won't become F+.

Also :

What is particularly interesting about the F+ factor is the fact that there seem to be a number of different kinds. An F+ factor making a bacterium fertile with some F- cultures does not necessarily make it capable of conjugating with others (49).

So not every F+ cell can conjugate with another F- cell.


Miraculous Microbes: They Make Holy Statues "Bleed"--and Can Be Deadly, Too

The Killer Bacteria Hall of Fame no doubt houses the usual suspects: Yersinia pestis, perpetrator of the Plague Treponema pallidum, the spiral-shaped culprit in syphilis and Vibrio cholerae, the swimmer that causes cholera. But you have probably never heard of one of the inductees.

Serratia marcescens is a forgotten but ubiquitous bacterium that can produce a red pigment called prodigiosin and likes to hang out as a pink film in the shower grout and toilet bowls of less-than-scrupulously clean homes. The pigment is so persistent that giant amoebas called slime molds that dine on S. marcescens turn red just as flamingoes that eat shrimp turn pink. Yet the picture emerging of this unsung organism is increasingly sinister.

These bacterium first attracted scientific attention in early modern times when it was found oozing out of damp Italian statues, communion wafers and, of all things, polenta doing its best impersonation of "blood." And blood it was taken to be&mdashusually miraculously&mdashuntil a pharmacist named Bartolomeo Bizio started trying to get to the bottom of what peasants declared to be an outbreak of diabolically cursed polenta in 1819.

Bizio believed a microorganism was responsible. In the test chamber, he found the bacterium happily chowing down on polenta while cranking out red pigment. Believing it to be a fungus, he named it Serratia in honor of Italian physicist Serafino Serrati, and marcescens because of the pigment's tendency to fade or decay rapidly.

Fast forward to the middle of the 20th century. In the early 1950s the U.S. government decided it would be a good idea to use S. marcescens in a bioweapon dispersal experiment dubbed Operation Sea-Spray. They burst balloons filled with Serratia over San Francisco Bay. Chosen because the red pigment makes it easily traceable, the supposedly innocuous bacterium so generously sprinkled over the bay was subsequently linked to several respiratory infections and at least one death.

Since then the bacterium has been widely found to be an opportunistic human pathogen, capitalizing on its prowess in forming tight-knit surface communities called biofilms wherever it can. It infects urethras through catheters, lungs via respirators, and premature babies by way of hospital caregivers. S. marcescens turns out to be one of the top 10 causes of all hospital-acquired respiratory, neonatal and surgical infections, said Robert Shanks, associate professor of ophthalmology at the University of Pittsburgh School of Medicine, who studies S. marcescens.

It has also been found irritating or infecting the corneas of contact lens wearers who fail to clean their cases with enough diligence (or at all). "What I think is sort of strange about S. marcescens is so many people have them in their contact lens cases," said Regis Kowalski, an ocular microbiologist at the University of Pittsburgh Medical Center. Although it often lives there harmlessly, S. marcescens is the third-most common cause of ocular keratitis, a corneal infection usually caused by poorly cleaned cases.

Disturbingly, the bacterium also seems to thrive in soap and other aggressive cleaners. In your hand soap, you might have Serratia living in it," Shanks said. "We actually had a bottle of Triton X-100 that was contaminated with it. It was really hard to believe because it's a strong detergent." The many hospital outbreaks of Serratia, he added, are almost always traced to contaminated cleaning solutions.

Yet S. marcescens also has a benign side. Certain strains are a normal, harmless component of mammalian guts, water and soil, and probably pose little risk to your average healthy human who cleans his or her lens case properly.

But Serratia has doubled down the menace in the past few years. Just this year, nine patients died and another 10 were sickened in Alabama by feeding tubes and bags contaminated with S. marcescens. And you may recall the debacle that ensued in 2004 when Chiron Corp. had to deep-six some 48 million doses of flu&mdash half that year's &mdashat the beginning of the flu season due to unspecified contamination. The contaminant? Serratia marcescens.

And lately, rampaging Serratia have turned up in some even less expected places. In 2002 scientists discovered the "white pox" pathogen devouring elkhorn coral in the Caribbean was none other than S. marcescens. Although Serratia is a common inhabitant of beaches, canals and some shore-dwelling animals, it is not typically found in seawater, so discovering it there was a surprise, said Kathryn Sutherland, associate professor of biology at Rollins College in Winter Park, Fla., who unmasked the pathogen.

After extensive testing of Serratia strains from nearly every conceivable source, Sutherland and her colleagues concluded that the coral-killing strain was an exact match with one of the many strains found in human excrement. In a paper published in PloS ONE in August, they showed that this strain of bacteria experimentally caused white pox on elkhorn coral infected in the lab (although other factors such as another pathogen, pollution and rising water temperatures may also contribute to the disease, she noted).

Released from leaking septic systems ill-suited to the local geology of the Florida Keys, the bacterium by chance happened to be able to both survive in saltwater and dine on elkhorn coral, an unhappy accident for both us and it, because about 90 percent of the species in those waters have vanished in the last 15 years. "I call them elkhorn graveyards," she said of the ghostly fields of departed coral.

The story does not stop there. In 2010 scientists reported a bacterium from the genus Serratia partnering with microscopic roundworms called nematodes from the genus Caenorhabditis&mdashthe genus to which C. elegans, a much-loved experimental subject, belongs&mdashto take out insects. Recent research had already indicated C. elegans was not the sweet little free-living soil dweller scientists may long have thought they had cultured. Instead, nematodes in this genus make a living by hitching rides on insects to travel between food sources or by living on them and patiently waiting for them to die so they can feast on the corpse.

But a chance encounter revealed a darker story. Discovered accidentally in a wax moth larvae&ndashbaited nematode trap in South Africa, scientists discovered a new species of roundworm called C. briggsae had partnered with a species of Serratia. In these sorts of relationships, which also occur in other nematode genera, symbiotic bacteria are carried inside the nematode's digestive tract, sometimes in pouches especially for the purpose.

Bacteria-loaded nematodes invade an insect through its own digestive openings or cuticle pores. Once inside, the roundworms release the bacteria, which start releasing toxins. "The bacteria does the work of the killing and changing the whole thing into a septic soup," said Eyualem Abebe, a biologist at Elizabeth City State University in North Carolina and lead author of the study that discovered the Serratia&ndashCaenorhabditis partnership. The nematodes, in turn, feast on the bacteria in an arrangement that could be looked at as a twisted agricultural scheme. Intriguingly, the researchers also found that by adding the requisite strain of Serratia to five other non&ndashinsect infecting Caenorhabditis species&mdashincluding the venerable C. elegans&mdashthey were able to turn all these freeloaders into killers.

How is it that Serratia can survive in so many different environments and opportunistically infect so many unrelated hosts? Shanks thinks it is because Serratia is a classic bacterial generalist. It has a big genome packing enough genes to consume practically any carbon (food) source and to resist virtually any antibiotic&mdashtraits acquired through countless generations of selection in bacterial soil wars. "It's got so many enzymes it can eat just about anything," he said.

Which brings up one final question: Just what is that red pigment that Serratia sometimes secretes, and why does it make it? Until recently, few had bothered to investigate that question. The research of Pryce Haddix, associate professor of biology at Auburn University at Montgomery, suggests the bacterium may be using the pigment to slow energy production in the form of ATP (adenosine triphosphate) and limit damage from free radicals caused by oxygen's presence during ATP synthesis as it prepares for rest or dormancy, he said.

But why red? Does the bloody hue have a physiologic purpose or is the bacteria's sinister appearance merely a chemical coincidence? "That's an excellent question," he said. "I don't have a clue really."


24 thoughts on &ldquo Oral bacteria may be responsible for Alzheimer’s disease &rdquo

My husband who has Alzheimers for the past 2 years was treated for gum disease 20 years ago. Do they think its a previous infection or a current infection. Are there any clinical trials expected?
Thank you

Hi Mary,
My mother had Alzheimer’s disease. The nursing home where she was supposed to be looked after more than often didn’t feed her decent food and her weight went down so much that she was only skin and bone and she wouldn’t talk except to “the pain”.
I asked the manager of the nursing home how long she had to live and they told me about a week.
When I arrived home, I pleaded with all my heart and soul to God for an answer. IO loved my mother and I didn’t want her to die.
God gave me an answer, and I heard it clearly from Him in just one word, “Nourishment”.
MY sister had given me the book “Raw Energy by Leslie Kenton” and I had been on it quite some time ago and knew how great it makes you feel, so I decided to feed my mother with all raw foods apart from fish which had to be cooked.
Because the nursing home had lost my mother’s false teeth, I had to blend everything in a drink, or cut it up so small that she didn’t need to chew it.
I noticed that within a week she had improved quite a lot, and after a month, she was chatting and happy, but still very weak in strength.
Continuing on with the diet and making sure that she had all the necessary nutrients, my mother seemed to be back to her old self, laughing and joking and talking about all sorts of things.
I had my mother for another three years and three months, but the nursing staff let her fall out of bed onto the ceramic floor when they came to wash her and the fall broke her ankle and wrist. The nursing home manager said that they had a doctor examine her and that the swelling was lasix in the blood.
This is when the nursing home gave her Panadol for pain relief. My mother was put on a morphine drip and she died
a few days later when I saw the give her five pumps of morphine.
My sister came down from Queensland and because the plane was late she didn’t get to see my mother while she was still alive, but examined my mother a few moments after she died and said that our mother’s wrist and ankle were broken. ( something we weren’t told about).
Don’t leave anyone in the care of a nursing home without watching carefully that they are fed and cared for properly.
God bless you.

Looks like this nursing homeshould be investigated. First they were under nourishing her then they dropped her and she broke broke her wrist and angle. This is all negligence and therefore accountable.

Hi Mary, this is the clinical trial for the chemical that may neutralize the bacterial toxin mentioned in the article. https://clinicaltrials.gov/ct2/show/NCT03331900 I don’t think we know enough about this bacteria and Alzheimer’s to answer your question unfortunately.

Are there any positive benefits from using drugs such as inbexa , donecept. And resperidone in the treatment of alzheimers

alzheimers is so terrible..
I hope we will never attacked by that disease..

Being so certain n relaxed that Alzheimer will never attack us is not fair,for that matter it can affect any one with aging,may be that in some people it comes as early as at 50 age n in some
as late as 90 which is taken as normal regressive phenomena. The exact etiology n pathophysiology is not verified as till date but with due time it may be established with causes.

Veerasak, I’ve been doing some research in herbs, and I might have found something promising. Any chance I could get your thoughts on the subject via email? Thank you for your time!

I am very interested to see what comes of this study. I am a dental hygienist and have been wondering if there is a link for the past few years. I have had a few patients over the years diagnosed with Alzheimer’s/Dementia and I started to notice some of them with uncontrolled periodontal disease or what seemed to be more aggressive bacteria present. It’s hard to say if this was always present or lack of homecare due to the disease. It makes me want to keep closer watch on my patients and their health histories. I’m hopeful this is getting closer to a cure.

An alzhemeir patient needs a care from a person. And also gives up his oral care. The person who takes care of him usually gets tire and can ignore the cleaning of teeth, so mouth. So giving up dental care results with an increasing amount of bacteria…

True statement. Lots of patients who don’t use the arms have bad oral health due to people ignoring the oral care. Lots of patients who have dementia will not let you brush their teeth.

Alzheimer’s is a major problem that the global medical community needs to find a way to treat

Interestingly, I did not think there was such a connection. They really need to think about Alzheimer’s

I think this is probably the best game. It was the best of life, even if it was just a shaky time. starvegas

How is P. Gingivalis eliminated? Is there an antibiotic that destroys the bacteria? Peroxide? Special mouthwashes?

Does the regular use of a mouthwash (e.g. Listerine) prevent these bacteria from settling in a person’s mouth?

I’m curious how much of the [email protected] program lead to the current knowledge in the study of Alzheimers.

Do you have any experience with treatment using the keto diet? There’s a lot of dementia in my family and I always forgot my keys, wallet and phone, but after dropping all carbs I have a much better memory.

Hi Tony,
My mother had Alzheimer’s disease. The nursing home where she was supposed to be looked after, more often than not, didn’t give her food that she could eat, and if she hadn’t eaten it in ten minutes, the plate of food was taken away. It didn’t matter to them that she couldn’t feed herself, or that she was a vegetarian and didn’t eat meat, so her weight went down so much that she was only skin and bone and eventually, she wouldn’t talk. I asked the manager of the nursing home how long she had to live and they told me about a week. When I arrived home, I pleaded with my whole heart and soul to God for an answer. I told Him that I love my mother and I don’t want her to die. It took a lot of pleading and crying but I kept a it until God gave me an answer, and I heard it clearly from Him in just one word, “Nourishment”. It came to me supernaturally.
MY sister had given me the book “Raw Energy by Leslie Kenton” and I had been on that diet quite some years ago, so I knew how great it makes you feel and look. That’s why I decided to feed my mother with all raw foods apart from the fish which had to be cooked.
Because the nursing home had lost my mother’s false teeth, I had to blend everything into a drink, or cut it up so finely that she didn’t need to chew it. It didn’t help that they brought in dried toast and an egg for her breakfast each morning or that they didn’t feed her the food that I had prepared and brought in for them to give her for her evening meals. When I asked for the week’s food containers, I was told that they were in the refrigerator, and of course, they were full of food, so my mother had only one meal a day.
I noticed that within a week she had improved quite a lot, and after a month, she was chatting and happy, but still very weak in strength. Continuing on with the diet and making sure that she had all the necessary nutrients, my mother seemed to be back to her old self again, laughing and joking and talking about all sorts of things. I had my mother for another three years and three months, but the nursing staff let her fall out of bed onto the ceramic floor when they came to wash her. The fall broke her ankle and wrist, and they had her lying on the side where she had most of the bruising so that we wouldn’t notice how bad it really was. The nursing home matron said that the doctor came in to examine my mother, and he said that the swelling was Lasix in the blood.
When my mother crossed her arms and wouldn’t put them down, I asked her what was wrong and she said “the pain”. This is when the matron told me that they gave her Panadol for the pain relief. I told them that my mother needs to go to the hospital for treatment, but they wouldn’t allow it because her husband who had since died, had filled in a form that she wasn’t to go into the hospital. My mother was put into Palliative Care and she was put on a morphine drip. She died a few days later after I saw the nurse give her five pumps of morphine. My sister came down from Queensland and because the plane was late she didn’t get to see my mother while she was still alive, but she examined mum a few moments after mum had died and she said that our mother’s wrist and ankle were broken, (that’s something we weren’t told about).
Please don’t leave anyone in the care of a nursing home without watching carefully that they are given enough to drink and are fed and cared for appropriately. God bless you and your family and I praise God for His answer to my prayers.
Valerie.

How can this bacteria be eliminated, perixode, antibiotics?

Hi Gayle,
While antibiotics may sometimes be necessary, however, depending on what they are used for, they are not taken without risks.
Antibiotics get rid of your good gut bacteria as well as your bad gut bacteria, and it takes at least two years or more to get your good bacteria to come back, but just as it takes many years for a rain forest to recover from the devastation of a fire, so it takes many years for your immune system to recover from antibiotics.
When taking antibiotics, you would be wise to take acidophilus as well, to help your immune system to recover more easily.
If you’ve already been on antibiotics, maybe you should speak to your health care professional about taking prebiotics to help to feed and replenish your good gut bacteria, but don’t take probiotics or you could have a nasty reaction to them because they feed the bad gut bacteria which feeds on the good gut bacteria.
Your skin is an organ and toxins are removed through your skin. so you can end up with a nasty itching rash like eczema or psoriasis that can exist for quite a long time.
Back in the year l903, a very soft toothbrush was used with a little salt in cool, boiled, distilled, and filtered rain water to brush the teeth and gums after each meal, and then the mouth was rinsed out with the rest of the salty water.

I need to correct some mistakes that showed up on my comment before it’s published. 1. to say the pain. 2. 1 instead of IO.

There were some typing errors in my reply which need to be corrected as I mentioned above.
My reply to Tony is the correct one.
The reply to Mary Foley had the typing errors that need to be changed.

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ELi5: Why can’t you boil a sponge to sanitize it?

Googling repeatedly tells you to just buy a new kitchen sponge, never boil them because it doesn’t work. But why wouldn’t it clean them?

12 2 9 & 6 More

Boiling or microwaving will KILL the bacteria. What it won't do is REMOVE the dead bacteria. That means there is dead biological material that's just food for more bacteria. The more you sanitize the sponge, the faster more new bacteria will grow. ELI5-when you kill bacteria it becomes bacteria food.

Edit: Wow. So. Heat, UV, bleach & desiccation(alcohol/sanitizer) can all kill bacteria. But there is no practical way to clean the material out of the deep pores of a sponge without destroying it. Nothing is as good as a clean sponge.

A short video of a single celled organism dying that demonstrates this concept:
https://www.youtube.com/watch?v=4bj6SqgT4SQ

DISCLAIMER: I am by no means a subject matter expert nor do I represent big sponge corp.


The survival of many organisms living in the ecosystems of the world depends on the ability of other organisms to convert inorganic compounds into energy that can be used by these and other organisms. Plants, algae, and bacteria have the ability to use sunlight, water, and carbon dioxide (CO2) and convert them into organic compounds necessary for life in a process called photosynthesis. Photosynthesis may take place in marine or terrestrial environments where the producing organisms are able to use sunlight as a source of energy.

Chemosynthesis occurs in environments where sunlight is not able to penetrate, such as in hydrothermal vents at the bottom of the ocean, coastal sediments, volcanoes, water in caves, cold seeps in the ocean floor, terrestrial hot springs, sunken ships, and within the decayed bodies of whales, among many others. Chemosynthetic bacteria use the energy stored within inorganic chemicals to synthesize the organic compounds needed for their metabolic processes.


Summary

  1. Physical control includes such methods of control as high or low temperature, desiccation, osmotic pressure, radiation, and filtration.
  2. Chemical control refers to the use of disinfectants, antiseptics, antibiotics, and chemotherapeutic antimicrobial chemicals.
  3. Sterilization is the process of destroying all living organisms and viruses.
  4. Disinfection is the elimination of microorganisms, but not necessarily endospores, from inanimate objects or surfaces.
  5. Decontamination is the treatment of an object or inanimate surface to make it safe to handle.
  6. A disinfectant is an agents used to disinfect inanimate objects but generally to toxic to use on human tissues.
  7. An antiseptic is an agent that kills or inhibits growth of microbes but is safe to use on human tissue.
  8. A sanitizer is an agent that reduces microbial numbers to a safe level.
  9. An antibiotic is a metabolic product produced by one microorganism that inhibits or kills other microorganisms.
  10. Synthetic chemicals that can be used therapeutically.
  11. An agent that is cidal in action kills microorganisms.
  12. An agent that is static in action inhibits the growth of microorganisms.
  13. Selective toxicity means that the chemical being used should inhibit or kill the intended pathogen without seriously harming the host.
  14. A broad spectrum agent is one generally effective against a variety of Gram-positive and Gram-negative bacteria.
  15. A narrow spectrum agent generally works against just Gram-positives, Gram-negatives, or only a few bacteria.

How do bacteria become resistant to antibiotics?

When you are fighting off a bacterial infection, your immune system can be overwhelmed by the invading bugs. Antibiotics are thrown into the fray to mount a defense against the invaders until your immune system can recover and finish off the remaining bacteria.

How do antibiotics stave off bacterial growth? Antibiotics stop or interfere with a number of everyday cellular processes that bacteria rely on for growth and survival, such as:

  • crippling production of the bacterial cell wall that protects the cell from the external environment
  • interfering with protein synthesis by binding to the machinery that builds proteins, amino acid by amino acid
  • wreaking havoc with metabolic processes, such as the synthesis of folic acid, a B vitamin that bacteria need to thrive
  • blocking synthesis of DNA and RNA

Antibiotics stop working because bacteria come up with various ways of countering these actions, such as:

  • Preventing the antibiotic from getting to its target When you really don't want to see someone, you might find yourself doing things like hiding from them or avoiding their phone calls. Bacteria employ similar strategies to keep antibiotics at bay. One effective way to keep a drug from reaching its target is to prevent it from being taken up at all. Bacteria do this by changing the permeability of their membranes or by reducing the number of channels available for drugs to diffuse through. Another strategy is to create the molecular equivalent of a club bouncer to escort antibiotics out the door if it gets in. Some bacteria use energy from ATP to power pumps that shoot antibiotics out of the cell.
  • Changing the target Many antibiotics work by sticking to their target and preventing it from interacting with other molecules inside the cell. Some bacteria respond by changing the structure of the target (or even replacing it within another molecule altogether) so that the antibiotic can no longer recognize it or bind to it.
  • Destroying the antibiotic This tactic takes interfering with the antibiotic to an extreme. Rather than simply pushing the drug aside or setting up molecular blockades, some bacteria survive by neutralizing their enemy directly. For example, some kinds of bacteria produce enzymes called beta-lactamases that chew up penicillin.

How do bacteria pick up these drug-fighting habits? In some cases, they don't. Some bacteria are simply making use of their own inherent capabilities. However, there are many bacteria that didn't start out resistant to a particular antibiotic. Bacteria can acquire resistance by getting a copy of a gene encoding an altered protein or an enzyme like beta lactamase from other bacteria, even from those of a different species. There are a number of ways to get a resistance gene:

  • During transformation - in this process, akin to bacterial sex, microbes can join together and transfer DNA to each other.
  • On a small, circular, extrachromosomal piece of DNA, called a plasmid - one plasmid can encode resistance to many different antibiotics.
  • Through a transposon - transposons are "jumping genes," small pieces of DNA that can hop from DNA molecule to DNA molecule. Once in a chromosome or plasmid, they can be integrated stably.
  • By scavenging DNA remnants from degraded, dead bacteria.

Unfortunately, if a bacterium gets a resistance gene stuck into its chromosomal DNA or picks one up in a free-floating plasmid, all of its progeny will inherit the gene and the resistance it confers. Why do resistance genes persist and spread throughout bacterial populations? It's basically just Darwin's idea of the survival of the fittest, reduced to a microscopic level -- bacteria with these genes survive and outgrow susceptible variants. And our own less than judicious use of antibiotics actually selects for these resistant types! Here's how we contribute to the problem:


New Understanding

Sometimes, organisms which look incredibly different are actually closely related. Look at the graph below, describing the phylogenetic relationships between different groups of animals.

This cladogram shows different groups of animals, with the green shaded area representing reptiles, or the taxonomic group “Reptilia”. As is made clear by the picture, reptiles include a group of animals which is paraphyletic. This is a paraphyletic group because it excludes the mammals (“Mammalia”) and the birds (“Aves”). Both of these groups are descendants of the first animals with amniotic development, the “Amniota”. The Amniota, as a group, would include both the birds and the mammals, and would be monophyletic.

Many groups which we consider natural groups, like the reptiles, are actually paraphyletic. While they include many related animals and their ancestors, these paraphyletic groups fail to take into account the whole picture and the diversity of life. While many of these classifications were made in the days when animals were judged solely by their looks. When modern techniques like DNA analysis were able to inform the relationships between animals, new patterns were observed.

Undiscovered Species

Often, we don’t even know that a group we are discussing is paraphyletic. Many species in the world remain undiscovered, which makes them unable to be placed in a phylogeny. If a group doesn’t include all of the existent species, it is a paraphyletic group. A paraphyletic group is not necessarily wrong, as it does show the relationship between organisms and their descendants. However, in analyzing paraphyletic groups, scientists cannot get a full view of the relationships between animals.

Language

Wasps are Paraphyletic

Here, you can clearly see that what laypeople call “wasps” are actually a paraphyletic group which excludes the ants and the bees. When you think about it, it is easy to see how these insects are related to wasps, but it is still wrong to call an ant or a bee a wasp. Yet, according to genetic relationships between the animals, they should all be a part of the same phylogenetic grouping.

Language is a common barrier for evolutionary biologists, and creates many paraphyletic groupings. This is often done unconsciously, as we simply inherit our language from our parents and have to learn how to use it best. For example, while it is now recognized that ants and bees are actually a subset of the paraphyletic wasp grouping, we will always call them ants and bees. Ants will not be called “wingless wasps”, nor will bees become “hairy wasps”. Language has a tendency to stick, making paraphyletic groups more or less a requirement when discussing evolution and the relationships between species.

1. A researcher studying the evolution of flying animals groups a bat and a butterfly, and labels them “Things which fly”. What kind of group is this?
A. Paraphyletic
B. Polyphyletic
C. Monophyletic

2. The advent of modern DNA analysis techniques revealed many paraphyletic groups within the classification schemes backed by science. Why is DNA more revealing than other traits animals have?
A. DNA is unlikely to have a homoplasy.
B. DNA cannot produce mistaken phylogenies.
C. DNA is not more revealing than other methods.

3. In the lab, a scientist goes through pain-staking efforts to create an entirely synthetic species of bacteria. Although the synthetic bacteria looks and functions like a regular bacteria, it is composed of entirely synthetic, non-natural parts. Even the DNA is composed of unique nucleotides, not found in the animal kingdom. The scientist claims that the new bacteria is in a monophyletic group of its own. Is the scientist correct?
A. No, the group is paraphyletic
B. Yes
C. No, there could be other species


Ancient microbiome study discovers unknown types of gut bacteria

A new study published in the journal Nature is reporting on the broadest genomic analysis of ancient poo ever conducted. The research reveals clues to ancient gut bacteria compositions, detecting microbial species never before seen in modern microbiomes.

The study focused on eight authenticated human feces samples found in dry caves in southwestern USA and Mexico. Carbon dating indicated the samples were between 1,000 and 2,000 years old.

Nearly 500 microbial genomes were reconstructed as part of the study, with the researchers confident around 180 could be strongly associated with ancient human microbiomes. Amazingly, 39 percent of those microbial genomes were previously unknown, having never been detected in any modern human microbiome.

Aleksandar Kostic, senior author on the study, says the incredible microbial diversity in ancient gut microbiomes may be due to dietary variations. Industrialized agriculture has led to a lack of variety in crops, meaning our gut bacteria simply does not need to be as diverse as it was in the past.

"In ancient cultures, the foods you're eating are very diverse and can support a more eclectic collection of microbes," says Kostic. "But as you move toward industrialization and more of a grocery-store diet, you lose a lot of nutrients that help to support a more diverse microbiome."

To compare these findings to modern microbiomes the researchers gathered several hundred fecal samples from humans today. Half of the modern samples came from those in the US or Europe eating a Western diet and the other half were gathered from more isolated indigenous communities in places such as Tanzania, Peru and Mexico.

One intriguing finding was the presence of a bacterium called Treponema succinifaciens in every single ancient sample, however, it was not found in any modern Western microbiome. Previous research has detected this bacterium in the microbiome of isolated indigenous communities and it has been hypothesized to be a sign modern industrial human gut microbiomes have diverged from more traditional states.

Another interesting finding was the ancient microbiomes displayed a higher volume of enzymes called transposases, which essentially aid genetic adaptability to dynamic environmental conditions.

“We think this could be a strategy used by the microbes to adapt in an environment that shifts a lot more than the modern industrialized microbiome, where we eat the same things and live the same life more or less year-round,” explains Kostic. “By contrast, in an environment marked by change, the microbes might use this much larger collection of transposases to grab and collect genes that could help them adapt to the different environments.”

And while overall microbial diversity was higher in the ancient microbiome samples, there seemed to be some microbes conspicuously absent in the old poo. Akkermansia muciniphila, for example, was absent from all ancient samples and only rarely detected in non-Western modern samples. Prior studies have found increased volumes of Akkermansia muciniphila in people eating diets high in processed meat and sugar. This microbe is known to produce endotoxins associated with inflammation.

Meradeth Snow, a University of Montana anthropologist working on the study, says this kind of research offers important insights into diseases that affect people in modern Western societies.

"It's a symbiotic relationship,” says Snow. “But when we study people today – anywhere on the planet – we know that their gut microbiomes have been influenced by our modern world, either through diet, chemicals, antibiotics or a host of other things. So understanding what the gut microbiome looked like before industrialization happened helps us understand what's different in today's guts."

The next step for some of the researchers working on the project will be to investigate what the possible metabolic functions were for some of these ancient bacterial species. Kostic speculates it could be possible to use these newly reconstructed ancient genomes to resurrect some of these extinct species and work out how they were influencing ancient humans.

“If we can grow them in the lab, we can understand the physiology of these microbes much, much better,” says Kostic.


The future of therapeutic viruses

Modern technology has enabled us to understand more about the complexities of the microbial communities that are part of the human body. In addition to good bacteria, we now know there are beneficial viruses present in the gut, skin and even blood.

Our understanding of this viral component is largely in its infancy. But it has huge potential in helping us understand viral infections, and importantly, how to fight the bad ones. It could also shed light on the evolution of the human genome, genetic diseases, and the development of gene therapies.

This article is republished from The Conversation under a Creative Commons license. Read the original article.


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